To further confirm the inhibitory effect of Smad1 on overall p300 mediated p53‐acetylaiton, p53 mutants containing a non‐acetylated site mutation (7KR) were constructed, in which 7 lysine residues (K164, K370, K372, K373, K381, K382, and K386) regulated by p300 were converted to Arg (R).[39] Considering R175H has the highest occurrence in cancer patients among the hotspot p53 mutations,[40] the lentivirus expressing R175H was used to represent a missense mutant p53. This evidence concerns the gene SMAD1 and cancer.